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153. Disruption of estrogen signaling does not prevent progesterone action in the estrogen receptor alpha knockout mouse uterus

Author

Curtis, Sylvia W., Clark, James H., Myers, Page, and Korach, Kenneth S.

Subjects
Estrogen -- Receptors, Progesterone -- Receptors, Hormone receptors -- Research, Mice -- Physiological aspects, Science and technology
Abstract

Estrogen is known to increase progesterone receptor (PR) levels in the wild-type mouse uterus, and this estrogen induction was thought to be important for progesterone action through the PR. The estrogen receptor [Alpha] knockout (ERKO) mouse uterus was observed to express PR mRNA that cannot be induced by estrogen. Progesterone action was characterized to determine whether it was diminished in ERKO mice. The PR protein is present in the ERKO uterus at 60% of the level measured in a wild-type uterus. The PR-A and PR-B isoforms are both detected on Western blot, and the ratio of isoforms is the same in both genotypes. Although the level of PR is reduced in the ERKO uterus, the receptor level is sufficient to induce genomic responses, since both calcitonin and amphiregulin mRNAs were increased after progesterone treatment. Finally, the ERKO uterus can be induced to undergo a progesterone-dependent decidual response. Surprisingly, the decidual response is estrogen independent in the ERKO, although it remains estrogen dependent in a wild type. These results indicate that estrogen receptor [Alpha] modulation of PR levels is not necessary for expression of the PR or genomic and physiologic responses to progesterone in the ERKO uterus.

Published
1999

162. Generation and reproductive phenotypes of mice lacking estrogen receptor beta

Author

Krege, John H., Hodgin, Jeffrey B., Couse, John F., Enmarks, Eva, Warner, Margaret, Mahler, Joel F., Sar, Madhabananda, Korach, Kenneth S., Gustafsson, Jan-Ake, and Smithies, Oliver

Subjects
Beta adrenoceptors -- Research, Estrogen -- Receptors, Mice -- Genetic aspects, Science and technology
Abstract

Estrogens influence the differentiation and maintenance of reproductive tissues and affect lipid metabolism and bone remodeling. Two estrogen receptors (ERs) have been identified to date, ER[Alpha] and ER[Beta]. We previously generated and studied knockout mice lacking estrogen receptor [Alpha] and reported severe reproductive and behavioral phenotypes including complete infertility of both male and female mice and absence of breast tissue development. Here we describe the generation of mice lacking estrogen receptor [Beta] (ER[Beta] -/-) by insertion of a neomycin resistance gene into exon 3 of the coding gene by using homologous recombination in embryonic stem cells. Mice lacking this receptor develop normally and are indistinguishable grossly and histologically as young adults from their littermates. RNA analysis and immunocytochemistry show that tissues from ERE -/- mice lack normal ER[Beta] RNA and protein. Breeding experiments with young, sexually mature females show that they are fertile and exhibit normal sexual behavior, but have fewer and smaller litters than wild-type mice. Superovulation experiments indicate that this reduction in fertility is the result of reduced ovarian efficiency. The mutant females have normal breast development and lactate normally. Young, sexually mature male mice show no overt abnormalities and reproduce normally. Older mutant males display signs of prostate and bladder hyperplasia. Our results indicate that ER[Beta] is essential for normal ovulation efficiency but is not essential for female or male sexual differentiation, fertility, or lactation. Future experiments are required to determine the role of ER[Beta] in bone and cardiovascular homeostasis.

Published
1998

169. The Concise guide to pharmacology 2019/20: Nuclear hormone receptors

Author

Alexander, Stephen PH, Cidlowski, John A, Kelly, Eamonn, Mathie, Alistair, Peters, John A, Veale, Emma L., Armstrong, Jane F, Faccenda, Elena, Harding, Simon D, Pawson, Adam J, Sharman, Joanna L, Southan, Christopher, Davies, Jamie A, Coons, Laurel, Fuller, Peter, Korach, Kenneth S, and Young, Morag

Subjects
0301 basic medicine, Pharmacology, RM, Clinical pharmacology, Computer science, Databases, Pharmaceutical, Drug classification, Receptors, Cytoplasmic and Nuclear, Ligands, law.invention, 03 medical and health sciences, 030104 developmental biology, 0302 clinical medicine, Pharmaceutical Preparations, law, Summary information, Animals, Humans, Catalytic receptors, 030217 neurology & neurosurgery, The Concise Guide to Pharmacology 2019/20
Abstract

The Concise Guide to PHARMACOLOGY 2019/20 is the fourth in this series of biennial publications. The Concise Guide provides concise overviews of the key properties of nearly 1800 human drug targets with an emphasis on selective pharmacology (where available), plus links to the open access knowledgebase source of drug targets and their ligands (www.guidetopharmacology.org), which provides more detailed views of target and ligand properties. Although the Concise Guide represents approximately 400 pages, the material presented is substantially reduced compared to information and links presented on the website. It provides a permanent, citable, point-in-time record that will survive database updates. The full contents of this section can be found at http://onlinelibrary.wiley.com/doi/10.1111/bph.14750. Nuclear hormone receptors are one of the six major pharmacological targets into which the Guide is divided, with the others being: G protein-coupled receptors, catalytic receptors, enzymes and transporters. These are presented with nomenclature guidance and summary information on the best available pharmacological tools, alongside key references and suggestions for further reading. The landscape format of the Concise Guide is designed to facilitate comparison of related targets from material contemporary to mid-2019, and supersedes data presented in the 2017/18, 2015/16 and 2013/14 Concise Guides and previous Guides to Receptors and Channels. It is produced in close conjunction with the International Union of Basic and Clinical Pharmacology Committee on Receptor Nomenclature and Drug Classification (NC-IUPHAR), therefore, providing official IUPHAR classification and nomenclature for human drug targets, where appropriate.

Published
2019

170. THE CONCISE GUIDE TO PHARMACOLOGY 2019/20: G protein-coupled receptors

Author

Alexander, Stephen PH, Christopoulos, Arthur, Davenport, Anthony P, Kelly, Eamonn, Mathie, Alistair, Peters, John A, Veale, Emma L, Armstrong, Jane F, Faccenda, Elena, Harding, Simon D, Pawson, Adam J, Sharman, Joanna L, Southan, Christopher, Davies, Jamie A, Arumugam, Thiruma V, Bennett, Andrew, Sjogren, Benita, Sobey, Christopher, Wong, Szu Shen, Abbracchio, Maria P, Alexander, Wayne, Al-hosaini, Khaled, Back, Magnus, Beaulieu, Jean-Martin, Bernstein, Kenneth E, Bettler, Bernhard, Birdsall, Nigel JM, Blaho, Victoria, Bousquet, Corinne, Brauner-Osborne, Hans, Burnstock, Geoffrey, Calo, Girolamo, Castano, Justo P, Catt, Kevin J, Ceruti, Stefania, Chazot, Paul, Chiang, Nan, Chun, Jerold, Cianciulli, Antonia, Clapp, Lucie H, Couture, Rejean, Csaba, Zsolt, Dent, Gordon, Singh, Khuraijam Dhanachandra, Douglas, Steven D, Dournaud, Pascal, Eguchi, Satoru, Escher, Emanuel, Filardo, Edward, Fong, Tung M, Fumagalli, Marta, Gainetdinov, Raul R, de Gasparo, Marc, Gershengorn, Marvin, Gobeil, Fernand, Goodfriend, Theodore L, Goudet, Cyril, Gregory, Karen J, Gundlach, Andrew L, Hamann, Jorg, Hanson, Julien, Hauger, Richard L, Hay, Debbie, Heinemann, Akos, Hollenberg, Morley D, Holliday, Nicholas D, Horiuchi, Mastgugu, Hoyer, Daniel, Hunyady, Laszlo, Husain, Ahsan, Ijzerman, Adriaan P, Inagami, Tadashi, Jacobson, Kenneth A, Jensen, Robert T, Jockers, Ralf, Jonnalagadda, Deepa, Karnik, Sadashiva, Kaupmann, Klemens, Kemp, Jacqueline, Kennedy, Charles, Kihara, Yasuyuki, Kozielewicz, Pawel, Kreienkamp, Hans-Juergen, Kukkonen, Jyrki P, Langenhan, Tobias, Leach, Katie, Lecca, Davide, Lee, John D, Leeman, Susan E, Leprince, Jerome, Lolait, Stephen J, Lupp, Amelie, Macrae, Robyn, Maguire, Janet, Mazella, Jean, McArdle, Craig A, Melmed, Shlomo, Michel, Martin C, Miller, Laurence, Mitolo, Vincenzo, Mouillac, Bernard, Murphy, Philip M, Nahon, Jean-Louis, Norel, Xavier, Nyimanu, Duuamene, O'Carroll, Anne-Marie, Offermanns, Stefan, Panaro, Maria A, Pertwee, Roger G, Pin, Jean-Philippe, Prossnitz, Eric, Ramachandran, Rithwik, Reinscheid, Rainer K, Rondard, Philippe, Rovati, G Enrico, Ruzza, Chiara, Sanger, Gareth, Schoeneberg, Torsten, Schulte, Gunnar, Schulz, Stefan, Segaloff, Deborah L, Serhan, Charles N, Stoddart, Leigh A, Sugimoto, Yukihiko, Summers, Roger, Tan, Valerie, Thomas, Walter, Timmermans, Pieter BMWM, Tirupula, Kalyan, Tulipano, Giovanni, Unal, Hamiyet, Unger, Thomas, Vanderheyden, Patrick, Vaudry, David, Vaudry, Hubert, Vilardaga, Jean-Pierre, Walker, Christopher S, Ward, Donald T, Wester, Hans-Juergen, Willars, Gary B, Williams, Tom Lloyd, Woodruff, Trent M, Yao, Chengcan, Aldrich, Richard W, Becirovic, Elvir, Biel, Martin, Catterall, William A, Conner, Alex C, Davies, Paul, Delling, Markus, Di Virgilio, Francesco, Falzoni, Simonetta, George, Chandy, Goldstein, Steve AN, Grissmer, Stephan, Ha, Kotdaji, Hammelmann, Verena, Hanukoglu, Israel, Jarvis, Mike, Jensen, Anders A, Kaczmarek, Leonard K, Kellenberger, Stephan, King, Brian, Lynch, Joseph W, Perez-Reyes, Edward, Plant, Leigh D, Rash, Lachlan D, Ren, Dejian, Sivilotti, Lucia G, Smart, Trevor G, Snutch, Terrance P, Tian, Jinbin, Van den Eynde, Charlotte, Vriens, Joris, Wei, Aguan D, Winn, Brenda T, Wulff, Heike, Xu, Haoxing, Yue, Lixia, Zhang, Xiaoli, Zhu, Michael, Coons, Laurel, Fuller, Peter, Korach, Kenneth S, Young, Morag, Bryant, Clare, Farndale, Richard W, Hobbs, Adrian, Jarvis, Gavin E, MacEwan, David, Monie, Tom P, Waldman, Scott, Beuve, Annie, Boison, Detlev, Brouckaert, Peter, Burnett, John C, Burns, Kathryn, Dessauer, Carmen, Friebe, Andreas, Garthwaite, John, Gertsch, Jurg, Helsby, Nuala, Izzo, Angelo A, Koesling, Doris, Kuhn, Michaela, Ostrom, Rennolds, Papapetropoulos, Andreas, Potter, Lincoln R, Pyne, Nigel J, Pyne, Susan, Russwurm, Michael, Schmidt, Harald HHW, Seifert, Roland, Stasch, Johannes-Peter, Szabo, Csaba, van der Stelt, Mario, van der Vliet, Albert, Watts, Val, Anderson, Catriona MH, Broer, Stefan, Dawson, Paul, Hagenbuch, Bruno, Hammond, James R, Hancox, Jules, Inui, Ken-ichi, Kanai, Yoshikatsu, Kemp, Stephan, Thwaites, David T, Verri, Tiziano, University of Nottingham, UK (UON), Monash university, University of Cambridge [UK] (CAM), University of Bristol [Bristol], University of Greenwich, Ninewells Hospital and Medical School [Dundee], University of Edinburgh, Institut de Génomique Fonctionnelle (IGF), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Montpellier (UM)-Centre National de la Recherche Scientifique (CNRS), Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier), Institut de médecine moléculaire de Rangueil (I2MR), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-IFR150-Institut National de la Santé et de la Recherche Médicale (INSERM), Department of Drug Design and Pharmacology [Copenhagen] (ILF), Faculty of Health and Medical Sciences, University of Copenhagen = Københavns Universitet (KU)-University of Copenhagen = Københavns Universitet (KU), University of Córdoba [Córdoba], Neuroprotection du Cerveau en Développement / Promoting Research Oriented Towards Early Cns Therapies (PROTECT), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Robert Debré-Université Paris Diderot - Paris 7 (UPD7)-Institut National de la Santé et de la Recherche Médicale (INSERM), Novartis Institutes for BioMedical Research (NIBR), Institut Cochin (IC UM3 (UMR 8104 / U1016)), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Différenciation et communication neuronale et neuroendocrine (DC2N), Université de Rouen Normandie (UNIROUEN), Normandie Université (NU)-Normandie Université (NU)-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut de pharmacologie moléculaire et cellulaire (IPMC), Université Nice Sophia Antipolis (1965 - 2019) (UNS), COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-Centre National de la Recherche Scientifique (CNRS)-Université Côte d'Azur (UCA), ARVALIS - Institut du végétal [Paris], Laboratoire de Recherche Vasculaire Translationnelle (LVTS (UMR_S_1148 / U1148)), Université Paris 13 (UP13)-Université Paris Diderot - Paris 7 (UPD7)-Institut National de la Santé et de la Recherche Médicale (INSERM), Max Planck Institute for Heart and Lung Research (MPI-HLR), Max-Planck-Gesellschaft, Glaxo Smith Kline [Harlow], University of Antwerp (UA), Neuroendocrinologie cellulaire et moléculaire, European Synchrotron Radiation Facility (ESRF), Experimental Medicine and Immunotherapeutics [Cambridge, UK], Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University [Riyadh] (KSU), Department of Cardiology, Karolinska University Hospital, Karolinska Institutet [Stockholm], Université de Montpellier (UM)-Université Montpellier 1 (UM1)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Montpellier 2 - Sciences et Techniques (UM2)-Centre National de la Recherche Scientifique (CNRS), Department of Medical Sciences, Università degli Studi di Ferrara (UniFE), Department of Pharmacological Sciences and Biomolecular, University of Milan, Department of Molecular Biology Helen L. Dorris, The Scripps Research Institute, Département de Physiologie, Université de Montréal (UdeM), Department of Pharmacology, Université de Sherbrooke (UdeS), Departments of Physiology & Pharmacology, and Medicine [Calgary, Canada] (School of Medicine), University of Calgary, Centre National de la Recherche Scientifique (CNRS)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre National de la Recherche Scientifique (CNRS)-Université Nice Sophia Antipolis (... - 2019) (UNS), COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-Université Côte d'Azur (UCA), Université Paris Diderot - Paris 7 (UPD7)-Université Paris 13 (UP13)-Institut National de la Santé et de la Recherche Médicale (INSERM), Institute of Biochemistry, Medical Faculty, University of Leipzig, Department of Molecular and Biochemical Pharmacology, and Pleinlaan 2

Subjects
0301 basic medicine, RM, Databases, Pharmaceutical, Computer science, Drug classification, Pharmacology, Ligands, Receptors, G-Protein-Coupled, NO, law.invention, 03 medical and health sciences, Databases, G-Protein-Coupled, 0302 clinical medicine, law, Summary information, Receptors, Animals, Humans, Pharmacology & Pharmacy, The Concise Guide to Pharmacology 2019/20, ComputingMilieux_MISCELLANEOUS, G protein-coupled receptor, Clinical pharmacology, Science & Technology, Extramural, POTENT, Pharmaceutical Preparations, 3. Good health, 030104 developmental biology, Pharmaceutical, [SDV.SP.PHARMA]Life Sciences [q-bio]/Pharmaceutical sciences/Pharmacology, [SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC], Catalytic receptors, Life Sciences & Biomedicine, 030217 neurology & neurosurgery
Abstract

© 2019 The Authors. British Journal of Pharmacology published by John Wiley & Sons Ltd on behalf of The British Pharmacological Society. The Concise Guide to PHARMACOLOGY 2019/20 is the fourth in this series of biennial publications. The Concise Guide provides concise overviews of the key properties of nearly 1800 human drug targets with an emphasis on selective pharmacology (where available), plus links to the open access knowledgebase source of drug targets and their ligands (www.guidetopharmacology.org), which provides more detailed views of target and ligand properties. Although the Concise Guide represents approximately 400 pages, the material presented is substantially reduced compared to information and links presented on the website. It provides a permanent, citable, point-in-time record that will survive database updates. The full contents of this section can be found at http://onlinelibrary.wiley.com/doi/10.1111/bph.14748. G protein-coupled receptors are one of the six major pharmacological targets into which the Guide is divided, with the others being: ion channels, nuclear hormone receptors, catalytic receptors, enzymes and transporters. These are presented with nomenclature guidance and summary information on the best available pharmacological tools, alongside key references and suggestions for further reading. The landscape format of the Concise Guide is designed to facilitate comparison of related targets from material contemporary to mid-2019, and supersedes data presented in the 2017/18, 2015/16 and 2013/14 Concise Guides and previous Guides to Receptors and Channels. It is produced in close conjunction with the International Union of Basic and Clinical Pharmacology Committee on Receptor Nomenclature and Drug Classification (NC-IUPHAR), therefore, providing official IUPHAR classification and nomenclature for human drug targets, where appropriate.

Published
2019

174. Spontaneous Airway Hyperresponsiveness in Estrogen Receptor-α—deficient Mice

Author

Carey, Michelle A., Card, Jeffrey W., Bradbury, Alyce J., Moorman, Michael P., Haykal-Coates, Najwa, Gavett, Stephen H., Graves, Joan P., Walker, Vickie R., Flake, Gordon P., Voltz, James W., Zhu, Daling, Jacobs, Elizabeth R., Dakhama, Azzeddine, Larsen, Gary L., Loader, Joan E., Gelfand, Erwin W., Germolec, Dori R., Korach, Kenneth S., and Zeldin, Darryl C.

Published
2007
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181. A role for oestrogens in the male reproductive system

Author

Hess, Rex a., Bunick, David, Lee, Ki-Ho, Bahr, Janice, Taylor, Julia A., Korach, Kenneth S., and Lubahn, Dennis B.

Subjects
Estrogen -- Research, Fertility -- Physiological aspects, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Research shows that oestrogen plays a physiological role in male reproductive organs, with oestrogen shown to regulate luminal fluid reabsorption in the epididymis head. Infertility occurs when the vital function is disrupted and diluted sperm enters the epididymis. Environmental oestrogens may potentially have an adverse impact on male reproduction. Testosterone and oestrogen are both present in males and females, with male concentrations of oestrogen very high in semen but low in blood.

Published
1997

182. Estrogenic responses in estrogen receptor-alpha deficient mice reveal a distinct estrogen signaling pathway

Author

Das, S.K., Taylor, Julia A., Korach, Kenneth S., Paria, B.C., Dey, S.K., and Lubahn, Dennis B.

Subjects
Mice -- Genetic aspects, Estrogen -- Research, Cellular signal transduction -- Research, Science and technology
Abstract

Estrogens are thought to regulate female reproductive functions by altering gene transcription in target organs primarily via the nuclear estrogen receptor-[Alpha] (ER-[Alpha]). By using ER-[Alpha] 'knock-out' (ERKO) mice, we demonstrate herein that a catecholestrogen, 4-hydroxyestradiol-17[Beta] (4-OH-[E.sub.2]), and an environmental estrogen, chlordecone (kepone), up-regulate the uterine expression of an estrogen-responsive gene, lactoferrin (LF), independent of ER-[Alpha]. A primary estrogen, estradiol-17[Beta] ([E.sub.2]), did not induce this LF response. An estrogen receptor antagonist, ICI-182,780, or [E.sub.2] failed to inhibit uterine LF gene expression induced by 4-OH-[E.sub.2] or kepone in ERKO mice, which suggests that this estrogen signaling pathway is independent of both ER-[Alpha] and the recently cloned ER-[Beta].4-OH-[E.sub.2], but not [E.sub.2], also stimulated increases in uterine water imbibition and macromolecule uptake in ovariectomized ERKO mice. The results strongly imply the presence of a distinct estrogen-signaling pathway in the mouse uterus that mediates the effects of both physiological and environmental estrogens. This estrogen response pathway will have profound implications for our understanding of the physiology and pathophysiology of female sex steroid hormone actions in target organs.

Published
1997

183. Responses in the brain of estrogen receptor (alpha)-disrupted mice

Author

Shughrue, Paul J., Lubahn, Dennis B., Negro-Vilar, Andres, Korach, Kenneth S., and Merchenthaler, Istvan

Subjects
Mice -- Physiological aspects, Brain research -- Analysis, Estrogen -- Research, Science and technology
Abstract

These studies sought to determine if neurons in the estrogen receptor-[Alpha] knockout (ER[Alpha]KO) mouse brain concentrated 16[Alpha]-[125I]iodo-11[Beta]-methoxy-17[Beta]-estradiol (125I-estrogen), and if so, whether estrogen binding augmented the expression of progesterone receptor (PR) mRNA. Mice were injected with 125I-estrogen and cryostat sections thaw mounted onto emulsion-coated slides. After 30-90 days of exposure, cells with a nuclear uptake and retention of 125I-estrogen were observed in a number of ER[Alpha]KO mouse brain regions including the preoptic nucleus and arcuate nucleus of the hypothalamus, bed nucleus of the stria terminalis, and amygdala, although the number of labeled cells and intensity of nuclear concentration was markedly attenuated when compared with wild-type littermates. Competition studies with excess 17[Beta]-estradiol, diethylstilbestrol, or moxestrol, but not with R5020 or dihydrotestosterone, prevented the nuclear concentration of 125I-estrogen. To determine if the low level of estrogen binding was capable of regulating gene expression, in situ hybridization was used to evaluate PR mRNA in the brain. ER[Alpha]KO and wild-type mice were ovariectomized and treated with vehicle or 17[Beta]-estradiol, and brains were sectioned and hybridized with a PR cRNA probe. Analysis of hybridization signal revealed a similar, low level of PR mRNA in ovariectomized wild-type and homozygous mice, and a marked increase in expression after treatment of ovariectomized animals with 17[Beta]-estradiol, with the level of hybridization signal being significantly higher in wild-type animals when compared with ER[Alpha]KO mice. The results demonstrate that estrogen binds in the ER[Alpha]KO brain and is capable of modulating PR gene expression, thus supporting the presence and functionality of a nonclassical estrogen receptor.

Published
1997

184. Increased expression of the cardiac L-type calcium channel in estrogen receptor-deficient mice

Author

Johnson, Barry D., Zheng, Wei, Korach, Kenneth S., Scheuer, Todd, Catterall, William A., and Rubanyi, Gabor M.

Subjects
Estrogen -- Physiological aspects, Calcium channels -- Research, Ion channels -- Research, Biological sciences, Health
Abstract

Physiological research has established that estrogen receptors control membrane density in the cardiac L-type calcium channels of mice. Evidence indicates that less estrogen might increase the number of cardiac L-type calcium channels and encourage cardiovascular diseases. Experiments using cardiac myocytes from estrogen receptor-deficient male mice are described, together with electrocardiogram results.

Published
1997

185. Effect of testosterone and estradiol in a man with aromatase deficiency

Author

Carani, Cesare, Qin, Kenan, Simoni, Manuela, Faustini-Fustini, Marco, Serpente, Stefania, Boyd, Jeff, Korach, Kenneth S., and Simpson, Evan R.

Subjects
Gene mutations -- Health aspects, Cytochrome P-450 -- Genetic aspects, Growth disorders -- Genetic aspects, Estradiol -- Health aspects, Bones -- Growth
Abstract

The case of a man with excessive growth illustrates the role that estrogen plays in bone maturation. He continued to grow after the age of 18 and by the age of 31, his height was in the 97th percentile. At that time he was evaluated for persistent growth, infertility and bone pain. X-rays revealed that his bones had not matured and continued to grow. His testosterone concentration was normal and his condition was unchanged by six months of testosterone treatment. Genetic analysis revealed a mutation in the gene for cytochrome P-450 aromatase. When his height exceeded the 97th percentile he was treated with estrogen, which caused his bones to mature.

Published
1997

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